Fastigial nucleus cardiovascular response and brain stem lesions in the beagle

Changes in the excitatory cardiovascular response (heart rate, arterial blood pressure, left ventricular pressure, and LV dP/dt as an index of myocardial contractility) resulting from electrical stimulation of the cerebellar fastigial nucleus (FN) were recorded after placement of DC or radio-frequency lesions or after microinjections of kainic acid into brain stem areas that receive FN projections and have been shown to be involved in central cardiovascular control. FN-induced increases in heart rate, blood pressure, and contractility were reduced or abolished by lesions made in the restiform body or the A5 area, which is homologous to the catecholamine-containing region in cats and rats. Lesions in the paramedian reticular nucleus, rostral and caudal to obex, failed to reduce the FN cardiovascular response. Nucleus of the solitary tract lesions augmented the FN pressor response and tachycardia. Kainic acid (1 microliter of 100 mM solution) caused profound depression of heart rate, blood pressure, and contractility and reduced or eliminated the FN-induced cardiovascular response when injected into the A5 area, previously identified by the pressor response following electrical stimulation. We concluded from these observations that a descending fastigiobulbar sympathoexcitatory pathway courses through a previously identified A5 pressor area that is also capable of a depressor response when the cell bodies alone are activated.